eLife · 2021
Reduced antibody cross-reactivity following infection with B.1.1.7 than with parental SARS-CoV-2 strains.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Faulkner Nikhil, Ng Kevin W, Wu Mary Y, Harvey Ruth, Margaritis Marios, Paraskevopoulou Stavroula, Houlihan Catherine, Hussain Saira, Greco Maria, Bolland William, Warchal Scott, Heaney Judith, Rickman Hannah, Spyer Moria, Frampton Daniel, Byott Matthew, de Oliveira Tulio, Sigal Alex, Kjaer Svend, Swanton Charles, Gandhi Sonia, Beale Rupert, Gamblin Steve J, McCauley John W, Daniels Rodney Stuart, Howell Michael, Bauer David, Nastouli Eleni, Kassiotis George
Аннотация
BACKGROUND: The degree of heterotypic immunity induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains is a major determinant of the spread of emerging variants and the success of vaccination campaigns, but remains incompletely understood.
METHODS: We examined the immunogenicity of SARS-CoV-2 variant B.1.1.7 (Alpha) that arose in the United Kingdom and spread globally. We determined titres of spike glycoprotein-binding antibodies and authentic virus neutralising antibodies induced by B.1.1.7 infection to infer homotypic and heterotypic immunity.
RESULTS: Antibodies elicited by B.1.1.7 infection exhibited significantly reduced recognition and neutralisation of parental strains or of the South Africa variant B.1.351 (Beta) than of the infecting variant. The drop in cross-reactivity was significantly more pronounced following B.1.1.7 than parental strain infection.
CONCLUSIONS: The results indicate that heterotypic immunity induced by SARS-CoV-2 variants is asymmetric.
FUNDING: This work was supported by the Francis Crick Institute and the Max Planck Institute for Dynamics of Complex Technical Systems, Magdeburg.
METHODS: We examined the immunogenicity of SARS-CoV-2 variant B.1.1.7 (Alpha) that arose in the United Kingdom and spread globally. We determined titres of spike glycoprotein-binding antibodies and authentic virus neutralising antibodies induced by B.1.1.7 infection to infer homotypic and heterotypic immunity.
RESULTS: Antibodies elicited by B.1.1.7 infection exhibited significantly reduced recognition and neutralisation of parental strains or of the South Africa variant B.1.351 (Beta) than of the infecting variant. The drop in cross-reactivity was significantly more pronounced following B.1.1.7 than parental strain infection.
CONCLUSIONS: The results indicate that heterotypic immunity induced by SARS-CoV-2 variants is asymmetric.
FUNDING: This work was supported by the Francis Crick Institute and the Max Planck Institute for Dynamics of Complex Technical Systems, Magdeburg.